The induction of sister chromatid exchanges by environmental pollutants: relationship of SCE to other measures of genetic damage.

Sister chromatid exchanges (SCEs), induced by environmental pollutants from fossil fuel use, were measured in 2 cell systems, Chinese hamster ovary (CHO) cells and Chinese hamster primary lung cell cultures. The frequency of SCEs induced in these cell systems was related to other measures of genetic damage, namely mutations in CHO cells at the hypoxanthine-guanine phosphoribosyl transferase (HGPRT) gene locus and in bacteria (Salmonella mutagenicity test TA-98), produced by the same pollutants. The pollutants were divided into 2 classes: those produced in oxidizing combustion environments--extracts of particles from light-duty diesel cars, spark-ignition cars, and an automotive tunnel; and those produced in reducing environments--extracts from coke oven mains and condensates from a low BTU coal gasifier obtained either before or after cleanup of the process stream. Sister chromatid exchanges were induced by all pollutants without the addition of a rat liver microsomal fraction (S-9 mix), whereas S-9 mix was required to induce a positive response in the CHO/HGPRT assay for all pollutants. The pollutants produced in a reducing environment required metabolic activation by S-9 mix to be mutagenic in the Salmonella mutation assay. The addition of S-9 mix to pollutants produced in an oxidizing environment reduced the response in the Salmonella test. The relative genotoxic potency for each pollutant was determined for all 3 endpoints. The slopes of dose-response curves for each pollutant were plotted for each assay to compare relative potency. When the bacterial mutagenicity test was compared to either mammalian cell assay, SCE or CHO/HGPRT, there was little correlation between relative potencies. However, the data indicated that the responses in the 2 mammalian cell assays, SCE and CHO/HGPRT, showed similar relative responses to the pollutants. Differences in the requirement for S-9 mix seem to be related to both the chemical nature of the mixture and the endpoint measured. Differences in responses are related not only to cell type but also to chemical composition of the complex pollutants.